In such cases, the anti-tumour mechanism of SLC41A1 was proposed to be Mg2+-dependent, with Mg2+ depletion by SLC41A1 overexpression resulting in Akt/mTOR inhibition and subsequent induction of Bax expression, triggering loss of membrane integrity and release of Cytochrome C to activate caspase-dependent apoptosis in PDAC (Figure 6C). The gene discussed is BAX; the disease is neoplasm.